Role of macrophages in vascular calcification: From the perspective of homeostasis.

Abstract

Vascular calcification (VC) is a crucial risk factor for the high morbidity and mortality associated with cardiovascular and cerebrovascular diseases. With the global population aging, the incidence of VC is escalating annually. However, due to its silent clinical process, VC often results in irreversible clinical outcomes. Inflammation is a core element in the VC process, and macrophages are the major inflammatory cells. Due to their diverse origins, microenvironments, and polarization states, macrophages exhibit significant heterogeneity, exerting strong effects on the occurrence, development, and even the regression of VC. In this review, we summarize the origin, distribution, classification, and surface markers of macrophages. Simultaneously, we explore the mechanisms by which macrophages maintain homeostasis or regulate inflammation, including the macrophage-mediated regulation of VC through the release of inflammatory factors, osteogenic genes, extracellular vesicles, and alterations in efferocytosis. Finally, we discuss research targeting inflammation and macrophages to develop novel therapeutic regimens for preventing and treating VC.